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DOWN SYNDROME HELPS RESEARCHERS UNDERSTAND ALZHEIMER'S DISEASE

The link between a
protein typically associated with Alzheimer's disease and its impact on memory
and cognition may not be as clear as once thought, according to a new study
from the University of Wisconsin-Madison's Waisman Center. The findings are
revealing more information about the earliest stages of the neurodegenerative
disease.

The researchers --
including lead study author Sigan Hartley, UW-Madison assistant professor of
human development and family studies, and Brad Christian, UW-Madison associate
professor of medical physics and psychiatry and director of PET Physics in the
Waisman Laboratory for Brain Imaging and Behavior -- looked at the role of the
brain protein amyloid-β in adults living with Down syndrome, a genetic
condition that leaves people more susceptible to developing Alzheimer's. They
published their findings in the September issue of the journal Brain.

"Our hope is to
better understand the role of this protein in memory and cognitive
function," says Hartley. "With this information we hope to better
understand the earliest stages in the development of this disease and gain
information to guide prevention and treatment efforts."

However, the findings
of their study not only may help scientists better understand the condition as
it impacts those living with Down syndrome, but they are also relevant to
adults without the genetic syndrome.

"There are many
unanswered questions about at what point amyloid-β, together with other brain
changes, begins to take a toll on memory and cognition and why certain
individuals may be more resistant than others," says Hartley.

The UW-Madison
scientists, along with collaborators at the University of Pittsburgh, studied
63 healthy adults with Down syndrome, aged 30 to 53, who did not exhibit
clinical signs of Alzheimer's or other forms of dementia. They found that many
adults with Down syndrome had high levels of amyloid-β protein but did not
suffer the expected negative consequences of the elevated protein.

Alzheimer's disease is
the sixth leading cause of death in the U.S. People with Down syndrome are born
with an extra copy of the 21st chromosome, where the gene that codes for the
amyloid-β protein resides.

For the study, which
was conducted over the course of two days, researchers used magnetic resonance
imaging (MRI) and positron emission tomography (PET) scans to capture images of
the participants' brains. Twenty-two of the 63 participants had elevated levels
of amyloid-β but showed no evidence of diminished memory or cognitive function
when compared to those without elevated levels of the protein. The researchers
controlled for differences in age and intellectual level.

Similarly, when
assessed as a continuous measure, amyloid-β levels were not tied to differences
in memory or cognitive ability, such as changes in visual and verbal memory,
attention and language.

Hartley and Christian
also partnered with Marsha Mailick, interim vice chancellor for research and
graduate education and Vaughan Bascom and Elizabeth M. Boggs Professor, and UW
Alzheimer's Disease Research Center (ADRC) investigators on the study. With
funding from the National Institute of Aging, the researchers plan to follow
these 63 adults for the next several years, to continue to track the
accumulation of amyloid-β and its effects over time.

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